Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and Renal Injury in Rats.

Li MA; Jian Fei; Ying Chen; Bing Zhao; Zhi-tao Yang; Lu Wang; Hui-qiu Sheng; Er-zhen Chen; En-qiang Mao

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Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and Renal Injury in Rats.

Author: Li MA ¹ ; Jian FEI ² ; Ying CHEN ¹ ; Bing ZHAO ¹ ; Zhi-Tao YANG ¹ ; Lu WANG ¹ ; Hui-Qiu SHENG ¹ ; Er-Zhen CHEN ¹ ; En-Qiang MAO ¹
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1. Department of Emergency Medicine, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
2. Department of General Surgery, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Publication Type:Journal Article
MeSH: Animals; Ascorbic Acid; therapeutic use; Blotting, Western; Cell Adhesion Molecules; metabolism; Epithelial Cells; drug effects; metabolism; pathology; Immunohistochemistry; Kidney Tubules; drug effects; metabolism; pathology; Lectins, C-Type; metabolism; Male; Rats; Rats, Sprague-Dawley; Receptors, Cell Surface; metabolism; Shock, Hemorrhagic; complications; drug therapy; metabolism
From: Chinese Medical Journal 2016;129(14):1731-1736
CountryChina
Language:English
Abstract:
BACKGROUNDThe expression of dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) in renal tubular epithelial cells has been thought to be highly correlated with the occurrence of several kidney diseases, but whether it takes place in renal tissues during hemorrhagic shock (HS) is unknown. The present study aimed to investigate this phenomenon and the inhibitory effect of Vitamin C (VitC).
METHODSA Sprague-Dawley rat HS model was established in vivo in this study. The expression level and location of DC-SIGN were observed in kidneys. Also, the degree of histological damage, the concentrations of tumor necrosis factor-μ and interleukin-6 in the renal tissues, and the serum concentration of blood urea nitrogen and creatinine at different times (2-24 h) after HS (six rats in each group), with or without VitC treatment before resuscitation, were evaluated.
RESULTSHS induced DC-SIGN expression in rat tubular epithelial cells. The proinflammatory cytokine concentration, histological damage scores, and functional injury of kidneys had increased. All these phenomena induced by HS were relieved when the rats were treated with VitC before resuscitation.
CONCLUSIONSThe results of the present study illustrated that HS could induce tubular epithelial cells expressing DC-SIGN, and the levels of proinflammatory cytokines in the kidney tissues improved correspondingly. The results also indicated that VitC could suppress the DC-SIGN expression in the tubular epithelial cells induced by HS and alleviate the inflammation and functional injury in the kidney.